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2025 PACUPrep BCCCP Preparatory Course Acute Ischemic Stroke Management of Acute Ischemic Stroke

Lesson 22, Topic 4

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Management of Acute Ischemic Stroke

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Supportive Care in ICU Acute Ischemic Stroke

Supportive Care and Complication Monitoring in ICU Acute Ischemic Stroke

Learning Objective

Recommend appropriate ICU supportive care and monitoring to manage complications associated with acute ischemic stroke (AIS) and its therapies.

I. Mechanical Ventilation and Airway Protection

In severe acute ischemic stroke (AIS), impaired consciousness and bulbar dysfunction may necessitate early intubation. Appropriate ventilator management balances cerebral perfusion and intracranial pressure (ICP).

A. Indications for Intubation and Mechanical Ventilation

Glasgow Coma Scale (GCS) ≤ 8
Loss of airway reflexes (gag, cough)
Dysphagia with high aspiration risk
Refractory hypoxemia or hypercapnia

B. Ventilator Goals

Maintain arterial PaCO₂ 35–45 mmHg
Maintain SpO₂ ≥ 94% without hyperoxia
Avoid hypocapnia (which can cause cerebral vasoconstriction)
Avoid hypercapnia (which can cause ICP elevation)

C. Initial Ventilator Settings

Tidal volume: 6 mL/kg ideal body weight
Positive End-Expiratory Pressure (PEEP): 5–8 cm H₂O, titrate to oxygenation and hemodynamics
Fraction of Inspired Oxygen (FiO₂): Wean to ≤ 60% as tolerated

D. Sedation and Assessment

Use light sedation (e.g., Richmond Agitation-Sedation Scale [RASS] –2 to 0) to permit serial neurologic exams.
Perform daily sedation interruption when feasible.
Employ an analgesia-first approach (e.g., fentanyl) to minimize delirium.

E. Monitoring

Continuous capnography for end-tidal CO₂ (EtCO₂) trends
Arterial blood gas (ABG) analysis after any ventilator change
Frequent neurologic checks (e.g., National Institutes of Health Stroke Scale [NIHSS], pupil exam)
Consider invasive ICP monitoring in cases of malignant edema

Key Points: Ventilation

Early airway protection prevents hypoxemia and aspiration pneumonia.
Normocapnia optimizes penumbral perfusion; avoid aggressive hyperventilation.
Light sedation facilitates neurologic monitoring and may shorten ventilation duration.

Case Vignette

A 72-year-old with a left Middle Cerebral Artery (MCA) stroke presents with GCS 7 and drooling. He is intubated and placed on mechanical ventilation with a tidal volume of 6 mL/kg, PEEP 5 cm H₂O, and FiO₂ 50%. End-tidal CO₂ is maintained at 40 mmHg; an ABG confirms PaCO₂ of 42 mmHg. Daily sedation breaks allow for neurologic assessment, leading to the detection of new right-sided weakness.

II. Prevention of ICU‐Related Complications

Immobilized AIS patients face high risks for thromboembolism, stress ulcers, and nosocomial infections. Proactive prophylaxis reduces morbidity.

A. Venous Thromboembolism (VTE) Prophylaxis

Mechanical Methods:

Intermittent pneumatic compression (IPC) devices: First choice when bleeding risk is high.
Graduated compression stockings: Considered adjunctive only, not primary prophylaxis.

Pharmacologic Methods:

Pharmacologic VTE Prophylaxis Agents
Agent	Mechanism	Dose	Monitoring & Notes	Reversal
Unfractionated Heparin (UFH)	Potentiates antithrombin III, inhibiting thrombin (Factor IIa) & Factor Xa	5,000 units SC q8–12 h	Preferred if CrCl < 30 mL/min or high/fluctuating bleeding risk. aPTT not routinely needed for prophylactic doses.	Protamine sulfate
Low‐Molecular‐Weight Heparin (LMWH, e.g., Enoxaparin)	Primarily anti-Xa activity > antithrombin III potentiation	Enoxaparin: 40 mg SC q24h (30 mg SC q24h if CrCl < 30 mL/min)	Predictable kinetics, once-daily dosing. Consider anti-Xa level in obesity or severe renal dysfunction.	Partial with protamine sulfate

Timing and Pearls:

Delay pharmacologic prophylaxis for 24 hours after intravenous thrombolysis (tPA) if no hemorrhage is seen on follow-up CT scan.
Resume UFH or LMWH 12–24 hours post-thrombectomy, based on bleeding risk assessment.
Combine IPC devices with pharmacologic agents when deemed safe.

Key Points: VTE Prophylaxis

Enoxaparin offers convenience but requires renal dosing adjustments.
UFH is rapidly reversible, making it preferable when bleeding risk fluctuates or renal function is poor.

B. Stress‐Related Mucosal Bleeding Prophylaxis

Indications:

Mechanical ventilation > 48 hours
Coagulopathy (e.g., INR > 1.5, platelets < 50,000/µL)
Shock or vasopressor dependence

Agents:

Proton pump inhibitors (PPIs): e.g., Pantoprazole 40 mg IV q24h
H₂ receptor antagonists (H₂RAs): e.g., Famotidine 20 mg IV q12h

Monitoring and Pearls:

Assess for signs of GI bleeding (e.g., melena, hematemesis, coffee-ground emesis).
Check magnesium levels if long-term PPI use is anticipated.
Reassess daily and discontinue prophylaxis when risk factors resolve.

Key Points: Stress Ulcer Prophylaxis

Restrict PPI/H₂RA use to high-risk patients to minimize risks like Clostridioides difficile infection and pneumonia.
Daily risk reassessment is crucial to avoid unnecessary exposure to acid-suppressive therapy.

C. Infection Prevention Bundles

Figure 1: Core components of ICU infection prevention strategies.

Ventilator-Associated Pneumonia (VAP) Bundle:

Head-of-bed elevation to 30–45°
Daily sedation interruption and assessment for spontaneous breathing trials
Oral care with chlorhexidine
Use of endotracheal tubes with subglottic secretion drainage

Central Line-Associated Bloodstream Infection (CLABSI) Bundle:

Maximal sterile barrier precautions during insertion
Chlorhexidine skin antisepsis
Daily review of line necessity and prompt removal when no longer indicated

Catheter-Associated Urinary Tract Infection (CAUTI) Bundle:

Avoid indwelling urinary catheters; use only if essential.
Maintain a closed drainage system and ensure aseptic insertion.
Remove catheters as soon as clinically feasible.

Dysphagia Screening:

Perform a formal dysphagia screen before any oral intake to prevent aspiration.

Key Points: Infection Prevention

Bundle adherence requires multidisciplinary coordination (nursing, respiratory therapy, pharmacy, physicians).
Early dysphagia assessment is critical in stroke patients to reduce aspiration pneumonia risk.

III. Management of Iatrogenic Complications

AIS therapies, particularly anticoagulants and contrast media, can cause bleeding and renal injury. Prompt recognition and targeted management are essential to mitigate harm.

A. Anticoagulant‐Induced Bleeding

Recognition:

Acute neurologic decline or new focal deficits
Drop in hemoglobin/hematocrit with no obvious source of bleeding
Obtain urgent noncontrast head CT scan

Reversal Strategies:

Anticoagulant Reversal Agents
Agent	Indication	Dose	Notes
Protamine Sulfate	Unfractionated Heparin (UFH)	1 mg per 100 units of heparin administered in prior 2–3 hours (max 50 mg per single dose)	Administer slowly (e.g., over 10 min) to avoid hypotension. Contraindicated in true fish allergy. Partially reverses LMWH.
Prothrombin Complex Concentrate (PCC)	Warfarin; Off-label for DOACs	25–50 units/kg based on INR and type of PCC (3-factor vs 4-factor)	Monitor INR. Risk of thrombotic events. 4-factor PCC preferred for warfarin reversal.
Vitamin K	Warfarin (adjunct to PCC)	5–10 mg IV (slow infusion) or PO	Slow onset (6–24 hours for full effect). IV route has small risk of anaphylactoid reaction.
Idarucizumab	Dabigatran	5 g IV (as two 2.5 g infusions or boluses)	Specific monoclonal antibody fragment. Rapid onset.
Andexanet Alfa	Factor Xa inhibitors (Rivaroxaban, Apixaban)	Dose varies (low vs. high dose regimen) based on specific Xa inhibitor and time since last dose.	Recombinant modified human factor Xa. Risk of thrombotic events.

Pearls and Pitfalls:

Protamine fully neutralizes UFH but only partially reverses LMWH and has no effect on Direct Oral Anticoagulants (DOACs).
When available, use specific reversal agents (e.g., idarucizumab for dabigatran, andexanet alfa for factor Xa inhibitors) for DOAC-related bleeding.

Key Points: Anticoagulant Bleeding

Rapid imaging (noncontrast head CT) is crucial to guide intervention; do not delay reversal pending all lab results if clinical suspicion is high.
For warfarin-associated intracranial hemorrhage, PCC (preferably 4-factor) plus intravenous vitamin K provides rapid and sustained INR correction.

B. Contrast‐Induced Nephropathy (CIN) / Contrast-Associated Acute Kidney Injury (CA-AKI)

Risk Factors:

Baseline renal dysfunction (e.g., eGFR < 60 mL/min/1.73 m², particularly <30-45)
Diabetes mellitus (especially with pre-existing nephropathy)
Volume depletion or dehydration
Concomitant use of nephrotoxic medications
High contrast volume or use of high-osmolality contrast media
Advanced age, heart failure

Risk Mitigation:

Intravenous isotonic saline (e.g., 0.9% NaCl or Lactated Ringer’s) at 1–1.5 mL/kg/h for 3–6 hours before and 6–12 hours after contrast administration.
Consider N-acetylcysteine (NAC) 600–1200 mg PO q12h for 2 days, starting before contrast (evidence is mixed, but low risk).
Minimize total contrast dose; use low-osmolar or iso-osmolar contrast agents.
Hold potentially nephrotoxic medications (e.g., NSAIDs, metformin in some cases) peri-procedurally if safe.

Monitoring:

Serum creatinine at baseline and daily for 1–3 days post-procedure in high-risk patients.
Strict urine output charting.

Key Points: Contrast-Associated AKI

Adequate intravenous hydration with isotonic crystalloids is the cornerstone of CA-AKI prevention.
Identify high-risk patients pre-procedure and collaborate with radiology on strategies to minimize contrast exposure.

IV. Multidisciplinary Goals-of-Care Conversations

Early, structured discussions are crucial to align treatment with patient values and preferences, especially in scenarios of devastating AIS.

A. Timing and Triggers for Discussion

Evidence of large infarcts with malignant edema on imaging
Persistent poor neurologic status despite reperfusion therapies
Family request for prognosis or inquiry about limitations of care
Development of significant medical complications

B. Team Composition

Primary treating physician (Neurology, Neurocritical Care, or Critical Care)
Bedside nursing staff
Palliative care specialists (if available and appropriate)
Pharmacy (for symptom management discussions)
Social work and/or spiritual care

C. Communication Framework (e.g., SPIKES-adapted)

SPIKES Communication Framework

S Setting up the interview

P Perception (Patient’s/Family’s)

I Invitation (to share information)

K Knowledge (giving information)

E Empathy (addressing emotions)

S Strategy and Summary

Figure 2: The SPIKES framework for guiding difficult conversations.

Setting: Ensure a private, uninterrupted environment. Sit down.
Perception: Assess the family’s (or patient’s, if able) understanding of the situation (“What have you been told so far?”).
Invitation: Ask how much detail they wish to know (“How much information would you like me to share?”).
Knowledge: Share information clearly, concisely, and compassionately. Avoid jargon. Allow for silence and questions.
Empathy: Acknowledge and validate emotions and concerns (“I can see this is very upsetting.”).
Summary/Strategy: Summarize key points, discuss next steps, and revisit goals of care. Outline a plan.

D. Documentation

Clearly document advance directives, code status (e.g., DNR/DNI orders).
Record details of family meetings, including attendees, key discussion points, decisions made, and the agreed-upon plan of care.

Key Points: Goals-of-Care

Early involvement of palliative care can significantly support symptom management and complex decision-making.
Thorough and consistent documentation ensures that care aligns with patient and family wishes across all members of the healthcare team.

References

Powers WJ, Rabinstein AA, Ackerson T, et al. Guidelines for the Early Management of Patients With Acute Ischemic Stroke: 2019 Update to the 2018 Guidelines for the Early Management of Acute Ischemic Stroke. Stroke. 2019;50(12):e344–e418.
Robbins BT, Howington GT, Swafford K, et al. Advancements in the Management of Acute Ischemic Stroke: A Narrative Review of Current Evidence and Guidelines. JACEP Open. 2023;4(2):e12896.
Winstein CJ, Stein J, Arena R, et al. Guidelines for Adult Stroke Rehabilitation and Recovery: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association. Stroke. 2016;47(6):e98–e169.

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